Recent work has shown that a considerable polymorphism exists in collagen isolated from different tissues. Analysis of the collagen content of the major arteries has shown the presence of both Type I collagen (chain composition, (alpha 1 (I)) 2 alpha 2) and Type III collagen (chain composition, (alpha 1 (III)) 3). During the pathogenesis of atherosclerotic lesions a marked increase in collagen accumulation occurs, and which probably consists predominantly of Type I collagen. Initial experiments will be performed to identify the collagen types which can be isolated from cell cultures of medial smooth muscle, endothelial cells and adventitial fibroblasts obtained from the thoracic aortas of guinea pig and Rhesus monkey. Preliminary experiments have shown that cultured smooth muscle cells synthesize both Type I and Type III collagen, with the synthesis of Type III collagen often exceeding that of Type I collagen. A third collagenous peptide has also been isolated with an apparent molecular weight of 45,000. Preliminary experiments indicate that this peptide, designated CP45, is unrelated to other collagen types, and future experiments will involve a complete characterization of CP45 isolated both from smooth muscle cell cultures and from intact aortas. An attempt will be made to understand the functional role of CP45 in arterial structure, together with that of any additional minor collagen components which may be synthesized by these cells. At present definitive information does not exist concerning the contribution of different cell types to the collagen content of the intact aorta. By the use of cell culturing procedures the aorta can be effectively dissected into populations of its three major cell types, and the collagens synthesized by each cell type can be investigated separately. Opportunities will also exist for investigating possible control of collagen biosynthesis in each cell type, and to develop models to understand how changes in collagen biosynthesis may occur during the unscheduled proliferation of smooth muscle cells giving rise to atherosclerotic lesions.